Partial Plantar Fasciectomy With Autologous Platelet Concentrate

Chronic heel pain can be extremely complex and debilitating. Very subtle, and some not so subtle, lower extremity biomechanical compensations frequently occur resulting in symptom complexes that can be extensive and difficult to treat and not isolated to the heel. These multi-factorial pain syndromes can be confusing to the practitioner in the initial diagnosis and work up of the patient.

The American Podiatric Medical Association Practice Survey in 2003 found that up to 44% of patient visits to a foot and ankle practitioner every year present with a chief complaint of heel pain.1 The vast majority of these patients will be diagnosed with plantar fasciitis. No one really knows how many people are affected by heel pain. It has been estimated that greater than two million people every year in the United States suffer from heel pain and one study suggested 10 percent of the population.2 It has been estimated that 93% of all cases of heel pain can be attributed to plantar fasciitis (fasciopathy).

The etiology of heel pain can be complex and multi-factorial including such diagnoses (some erroneous) as plantar fasciitis/fasciosis, inferior calcaneal fat pad atrophy, infracalcaneal bursitis and medial calcaneal nerve entrapment. When misdiagnosed, the patient often receives unnecessary treatment including steroid injections and surgery. There is no current universal standard by which this diagnosis is made and also no agreed-upon staging and grading scheme to determine appropriate treatment.

Understanding the Heel

The human plantar fascia is a dense aponeurosis that originates from the inferior aspect of the calcaneus. It is often confluent anatomically with the distal insertion of the Achilles tendon fibers on the inferior surface of the calcaneus and provides the majority of the biomechanical structural support for the foot during stance and especially gait. It is dynamic and terminates distally in the forefoot and toes with a complex integration into the soft tissues of the fat pad on the sole of the foot and in the submetatarsal head area.3 The plantar fascia provides a critically important digital stabilization mechanism with subsequent offloading of the metatarsal heads during the late midstance and the propulsive phases of gait. The histology and appearance of the plantar fascia with high resolution diagnostic ultrasound is similar to that found for tendon4 (see Figure 1).

Chronic plantar heel pain has been documented to have a severe negative impact on the general quality of life as reported by Irving, et al in a 2008 article in the Journal of the American Podiatric Medical Association.5

Plantar Fasciopathy (Plantar Fasciosis)

While it is still generally and erroneously believed that the plantar fascia becomes chronically inflamed because it is subjected to an excessive mechanical axial tension that is subsequently often treated by the misguided use of steroids and NSAID’s, it is known that the condition is degenerative.6,7 In 2003, Lemont published a study in the Journal of the American Podiatric Medical Association,7 where it was objectively determined that the condition that has been mistakenly attributed to an inflammation of the plantar fascia is, in fact, a degenerative condition similar to tendinopathy. In specimens taken at the time of plantar fasciectomy, no histologic mediators of inflammation were seen microscopically. Similar findings in tendinopathy confirm what Lemont observed.8-10 This was further demonstrated in tendon animal studies.11 Histological separation and disruption of collagen fibrils both lengthwise and crosswise, an increase in tenocytes—combined with vascular hyperplasia—has been repeatedly observed. Visualization with high-resolution diagnostic ultrasound of this tissue response—as hypoechoic signal intensity—has been previously and erroneously attributed to inflammation within the tissue. An example of this can be seen in Figure 2.

Figure 2. Abnormally thickened plantar fascia with hypoechoic signal intensity. Tendon or aponeurosis can only handle an eccentric force to approximately 4-6% of its original length without pathologic damage occurring.12 This results in tissue breakdown within 2-3 weeks and is a degenerative rather than an inflammatory response.7 It is known that the plantar fascia can handle high tensile loads and has a stress modulus between that of ligament and tendon.1 The concept of high axial tension forces acting as the primary etiological factor in the development of this condition needs to be scrutinized. In strong support of the cause of plantar fasciosis more likely being due to compressive and shearing type forces, as opposed to axial ones, is Li and Muehleman’s histological study which demonstrated that the trabeculae within the inferior calcaneal exostosis are not aligned with the tension force of the plantar fascia (which has always been perceived to be the etiology of the breakdown of the plantar fascia) but instead are due to the stress placed on the inferior surface of the calcaneus with weight bearing.13 It is likely that within the first few weeks when the plantar fascia starts to become symptomatic, it may be initially due to an inflammatory response. However, it has been shown in animal studies that when the tendon is subjected to a lengthwise tensile force that stretches the tendon to more than its normal tolerance (which is only about 4-6 percent of its length), there are no cellular signs of inflammation after two to three weeks. These areas of tendonous or ligamentous structures that become damaged remain in this chronic state of degeneration unable to heal. The appearance of degeneration of the plantar fascia with ultrasound highly correlates to the symptomatic presentation of pain. However, people can have degeneration without pain just the same as people can have pain without degeneration. As can be seen in Table 1, the presence of hypoechoic signal intensity visualized in the substance of the plantar fascia is highly correlated with the presence of plantar fasciosis.

In light of these findings, more accurate nomenclature is now being widely used, and the condition we used to call plantar fasciitis is now more accurately referred to as “plantar fasciopathy” or “plantar fasciosis.”

Inferior Calcaneal Fat Pad Atrophy and Infracalcaneal Bursitis

Some patient’s heel pain can be attributed to an atrophy (usually from repeated corticosteroid injections for the treatment of plantar “fasciitis”) or disorder of the heel pad. This structure can be easily evaluated by diagnostic ultrasound both for its thickness, and compressibility. Several studies have determined that there is no significant difference in the fat pad between patients with plantar fasciosis and controls.21 This correlates to what we have seen clinically over the last decade and determined that measurement of fat pad dimensions has proven useless except in cases where there is known atrophy or prior destruction of the infracalcaneal fat pad. There has not been any correlation with heel pain and thickness of the fat pad measured by diagnostic ultrasound in our clinical experience.

There is much discussion in past literature dealing with plantar heel pain attributing the patient’s symptoms to an infracalcaneal bursitis. The author has never seen one in thousands of heels with diagnostic ultrasound imaging or MRI. Presence of fluid is readily appreciated with DUS and the likelihood of missing this on ultrasound examination is remote. In a study of 200 fresh frozen cadavers, no calcaneal bursae were identified but, in nearly every specimen, there was a consistent tissue plane between the most inferior aspect of the periosteum of the calcaneus where it interfaces with the central hydraulic chamber of the infracalcaneal fat pad and where it would be possible for fluid to accumulate.22 But again, this has never been seen in our vast clinical experience with DUS evaluation of heel pain over the last decade. This could be the tissue interface where Gibbon describes the visualization of peri fascial edema.16 However, in thousands of heel sonograms, the author has not seen a definitive accumulation of fluid at this tissue interface—any such fluid accumulation would be readily seen with this technology. The dogma of the infracalcaneal bursa was entrenched in the literature far before the advent of high resolution diagnostic ultrasound and clearly, if they occur, they are extremely rare.

Multiple Etiology Heel Pain Syndrome

There is no human physiological rule that prevents patients from having more than one pathological condition simultaneously. This is especially true with heel pain.

Frequently, patients will present with a multiple etiology heel pain syndrome (MEHPS). MEHPS is more common than many believe, with the most frequent association being entrapment of the medial calcaneal nerve(s) in conjunction with plantar fasciopathy.23 In Rose and Malay’s study, more than 72% of patients who initially presented with plantar fasciitis also had co-existing nerve entrapment of either the tarsal tunnel or medial calcaneal nerve as confirmed by neurosensory testing.24 Specifically, diagnostic high-resolution ultrasound can enable a practitioner to make more educated assessments of the true pain generator in complex heel pain and is cost efficient, expedient, and very beneficial for the patient.

The MEHPS questionnaire, while not a scientifically validated instrument, was developed to assist the clinician in understanding the patient’s symptoms and likely source of the heel pain. Table 2 presents the MEHPS questionnaire in its entirety as well as the scoring system that is used to guide diagnosis. Each foot is graded separately.

Probably multiple etiologies with both fasciosis and neurogenic etiology

>15 Points

Nerve entrapment or neurogenic etiology is likely the most significant contributor to the patient’s symptoms

Diagnostic Ultrasonography

The definitive diagnosis of plantar fasciopathy can be made with high-resolution diagnostic ultrasound, and supersedes any clinical evaluation methods currently available, including MRI.

Until recently many clinicians treating heel pain primarily relied on history of present illness, clinical evaluation, which usually consisted only of palpation of the medial calcaneal tubercle with their thumb, and simple x-rays (and many still do). It is widely espoused that conservative care is efficacious in 80-90% of all patients with plantar heel pain due to plantar fasciopathy.15 We can see from an analysis of the epidemiological numbers that, even if this were true, there would be thousands of patients that will undergo long periods of failed conservative care only to have continued heel pain, whereas, with use of sonography, treatment paradigms are changing. Over the last decade, the use of high-resolution diagnostic ultrasound has been widely integrated into clinical practices. It is clearly apparent, after evaluation of hundreds of patients presenting with plantar heel pain, that not all heel pain is caused by isolated problems with the plantar fascia and, in those who do have objective pathology of the plantar fascia, there are widely variable presentations in how their plantar fascia presents on ultrasound. Most practitioners can easily accept that all plantar fasciopathy (cases between different individual patients) is not the same as there are different levels of the disease as well as the location of the degeneration within the plantar fascia itself. However, sonographic visualization, in combination with focused examination, has allowed the development of an objective categorization or grading of the actual structural condition of the plantar fascia and ideally should lead to more tailored and specific treatment and ultimately improve patient outcomes. This grading system has not been scientifically validated, but has proven to be very accurate in the more than seven years of clinical practice (see Table 3). When the grading system was first devised, grades IC and IVA were included in the treatment model. Time has proven that even though these categories could theoretically exist, clinically they are very rarely, if ever, present.

Table 3. Clinical Grading System Used to Direct Treatment When Using Diagnostic Ultrasound to Evaluate the Thickness of the Plantar Fascia

Treatment

The overall concept, philosophy, and methodology—which include conservative care, minimally invasive and endoscopic treatments—are strongly focused on accurate and thorough diagnosis. In the treatment of heel pain, as it is with virtually everything else in medicine, nothing is more important than having an accurate diagnosis.

Initial treatments for heel pain may include biomechanical control with custom orthotic devices, soft silicone inserts to increase shock absorption, stretching exercises, occasional physical therapy modalities, and use of anti-inflammatory medications. It must be emphasized that each case is unique and that, with the use of diagnostic ultrasound, the patient can be assured that he or she will not undergo a long and ineffective course of conservative care—if severe pathology is recognized in the diagnostic phase of evaluation.

The authors recommend that cases of plantar fasciopathy graded initially within groups IIC through IIC be immediately treated with ultrasound-guided partial plantar fasciectomy (USGPPF) without extended periods of conservative care. This type of intervention does not interrupt the biomechanical function of the foot as procedures which involve fasciotomy do and therefore can be implemented without reservation about compromise of functional stability. It is completely safe to inject autologous platelet into musculoskeletal tissue with very minimal associated risks and hazards. Those cases which would be classified in the IVB and IVC grades can successfully have this type of intervention, but the patient needs to be educated that they may ultimately require a plantar fasciotomy.

As previously stated, ultrasound can be used effectively in the diagnosis of plantar fasciosis. It can also be utilized in augmenting treatment of it. By using ultrasound guidance to fenestrate, debride and place autologous platelet concentrate within the plantar fascia, the surgeon can be assured that the appropriate tissue is being treated. The following is the surgical technique used when treating plantar fasciosis with ultrasound-guided partial plantar fasciectomy, autologous platelet concentrate and extracorporeal shockwave therapy.

The patient is placed in a supine position. General anesthesia is recommended. 20cc of blood is drawn from the antecubital fossa in the preoperative area. This is mixed with 2cc of ACDA to prevent coagulation. Using the Harvest Technologies’ SmartPReP System, the blood is processed yielding approximately 3.5 cc of autologous platelet concentrate. During the processing time, the patient is locally anesthetized with a combination sural nerve and tibial nerve block at the level of the malleolus.

Figure 3. Topographical mapping of the planar fascia from imaging with the diagnostic ultrasound.Figure 4. The plantar fascial rasp.Using a high resolution, diagnostic musculoskeletal ultrasound with a 15 megahertz transducer, the patient’s plantar fascia is examined and mapped in both the sagittal plane and transverse plane (see Figure 3). Using a #11 blade, a 2mm incision is made just through the dermis. This allows for placement of the rasp without damage to the skin and potential for introduction of epidermal cells into deeper tissue. From a medial approach, a fascial rasp (see Figure 4) is introduced into the most hypoechoic areas of the medial and central bands of the plantar fascia (see Figure 5).

Figure 5. The rasp in the plantar fascia during debridement. The image on the left is taken while holding the transducer longitudinally and, in the image on the right, the transducer is held transversely.

As the rasp is introduced into the hypoechoic areas of the fascia, the diagnostic ultrasound is used for real time visualization (see Figure 5). The degenerative areas, which correspond visually with the hypoechoic areas, are scraped with the fascial rasp for partial excision of the plantar fascia. The surgeon will experience a psychomotor sensation as a result of less resistance to the fascial rasp when within the degenerated tissue. Better results will be achieved if the surgeon is aggressive with the debridement in the degenerative (hypoechoic) areas. After adequate partial fasciectomy of the medial and central bands, the autologous platelet concentrate is then infiltrated as a tissue graft substitute into the previously debrided and prepared areas of the plantar fascia. Distention and dissemination of the tissue transfer is noted visually on the ultrasound in real time, indicating proper placement of the APC graft (see Figure 6).

Figure 6. Application of the autologous platelet concentrate through a 25 gage needle.

Figure 7. Application of shockwave.Figure 8. After the procedure, an adhesive bandage is adequate; a bulky dressing is not required.

After completion of the tissue transfer, platelet activation is initiated with the Swiss DolorClast low energy radial extracorporeal shockwave machine (see Figure 7). 2000 shocks are delivered at the medial calcaneal tubercle with a consistent application pressure. Prior to shockwave application, a sterile occlusive/translucent dressing is applied. A sterile dressing is then applied to the medial heel (see Figure 8). Figure 9 illustrates a typical ultrasound of plantar fascia thickness and echogenicity of the plantar fascia before and after the procedure.

Figure 9. Plantar fascia thickness and echogenicity of the plantar fascia before and after.Results

Patients with plantar fasciosis in grades IIC – IIIC can expect nearly a 94% success rate with USGPPF. In a retrospective study of 74 patients who were not limited to these grades, 68 related an excellent/good outcome with no report of complications.

Summary/Discussion

Heel pain can be complex and must be thoroughly evaluated with both clinical means as well as with high-resolution diagnostic ultrasound since accurate diagnosis leads to improved patient outcomes. There is a very high success rate with USGPPF and infiltration with APC and activating shockwave—with virtually no complications. Patients must be educated that this is a regenerative procedure and that the ultimate beneficial result may take 6-8 weeks to achieve and that the procedure can actually increase their pain temporarily for several days. Additionally, patients must understand that this technique creates an inflammatory response that is necessary for healing to occur and that use of NSAIDs or other anti-inflammatory agents should not be used until at least three weeks after USGPPF. Most patients report a reduction of pain at less than pre-procedure levels at about two weeks post-procedure. Note that objective diagnostic imaging does not always directly correlate post-operatively with clinical status and there is no contraindication to repeat injection.

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